RESUMO
This study was conducted to identify the distribution of virulence determinants in uropathogenic Escherichia coli (UPEC) isolates obtained from kidney transplant (KTP) and non-transplant patients (non-KTP) with urinary tract infections (UTI). Additionally, the (GTG)5 fingerprinting technique was used to investigate the genetic diversity of Extended-Spectrum B-Lactamase (ESBL)-positive isolates. In this case-control study, 111 urine isolates were obtained from non-KTPs and KTPs, respectively. The presence of genetic markers encoding adhesion proteins, toxins and major E. coli phylogroups was assessed through PCR amplification. Molecular typing of ESBL-positive UPEC strains was performed using (GTG)5 fingerprinting and Multilocus sequence typing (MLST) techniques. Overall, 65 and 46 UPEC isolates were obtained from non-KTPs and KTPs, respectively. Among the studied isolates, traT (85.6%) gene was the most frequently observed virulence gene, followed by kpsMT (49.5%). Using the 80% cut-off point, all the 35 UPEC isolates were classified into four major clusters, namely A, B, C, and D. The majority of the Sequence Type (ST) 131 isolates belonged to cluster A. Additionally, three ST1193 isolates belonged to cluster A and phylogroup B2. Moreover, ST38, ST131 and ST10 were in different cluster. In general, we observed significant differences in the papA, ompT, sat, and vat genes between KTPs and non-KTPs. Furthermore, since all the isolates carried one or more virulence factors (VFs), these findings are concerning in the context of managing UTIs caused by the UPEC strain. Additionally, the distribution of ST and Clonal Complex (CC) among isolates in the main clusters revealed significant differences between MLST and (GTG)5 fingerprinting analysis.
RESUMO
Mycobacterium tuberculosis, Mycobacterium leprae, and non-tuberculous mycobacteria (NTM) are among the most significant human pathogens within the Mycobacterium genus. These pathogens can infect people who come into contact with biomaterials or have chronic illnesses. A characteristic pathogenic trait of mycobacteria is the development of biofilms, which involves several molecules, such as the GroEL1 chaperone, glycopeptidolipids, and shorter-chain mycolic acids. Bacterial behavior is influenced by nutrients, ions, and carbon sources, which also play a regulatory role in biofilm development. Compared to their planktonic phase, mycobacterial biofilms are more resilient to environmental stresses and disinfectants. Mycobacteria that produce biofilms have been found in several environmental studies, particularly in water systems. NTM can cause respiratory problems in individuals with underlying illnesses such as cystic fibrosis, bronchiectasis, and old tuberculosis scars. Mycobacteria that grow slowly, like those in the Mycobacterium avium complex (MAC), or rapidly, like Mycobacterium abscessus, can be pathogens. Infections related to biomaterials represent a significant category of biofilm-associated infections, with rapidly growing mycobacteria being the most frequently identified organisms. A biofilm produced by M. tuberculosis can contribute to caseous necrosis and cavity formation in lung tissue. Additionally, M. tuberculosis forms biofilms on clinical biomaterials. Biofilm formation is a major contributor to antimicrobial resistance, providing defense against drugs that would typically be effective against these bacteria in their planktonic state. The antibiotic resistance of biofilm-forming microbes may render therapy ineffective, necessitating the physical removal of biofilms to cure the infection. Recently, new approaches have been developed with potential anti-biofilm compounds to increase treatment effectiveness. Understanding biofilms is crucial for the appropriate treatment of various NTM diseases, and the recent discovery of M. tuberculosis biofilms has opened up a new field of study. This review focuses on the biofilm formation of the Mycobacterial genus, the mechanisms of biofilm formation, and anti-mycobacterial biofilm agents.
